Parkinson's Disease - Dysphagia

8/08/01 (Ansari)

RE: A 75 year old female with history of Parkinson's disease who presented with difficulty swallowing. 

Question: Why do patients with Parkinons's disease get dysphagia?

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Unique Identifier: 21092257 / PubMed Identifier: 11176964

Authors: Muller J. Wenning GK. Verny M. McKee A. Chaudhuri KR. Jellinger K. Poewe W. Litvan I.

Institution: Cognitive Neuropharmacology Unit, The Champlain Building, 6410 Rockledge Dr, Suite 600, Bethesda, MD 20817-1844, USA.

Abstract: BACKGROUND: Dysarthria and dysphagia are known to occur in parkinsonian syndromes such as Parkinson disease (PD), dementia with Lewy bodies (DLB), corticobasal degeneration (CBD), multiple system atrophy (MSA), and progressive supranuclear palsy (PSP). Differences in the evolution of these symptoms have not been studied systematically in postmortem-confirmed cases. OBJECTIVE: To study differences in the evolution of dysarthria and dysphagia in postmortem-confirmed parkinsonian disorders. PATIENTS AND METHODS: Eighty-three pathologically confirmed cases (PD, n = 17; MSA, n = 15; DLB, n = 14; PSP, n = 24; and CBD, n = 13) formed the basis for a multicenter clinicopathological study organized by the National Institute of Neurological Disorders and Stroke, Bethesda, Md. Cases with enough clinicopathological documentation for the purpose of the study were selected from research and neuropathological files of 7 medical centers in 4 countries (Austria, France, England, and the United States). RESULTS: Median dysarthria latencies were short in PSP and MSA (24 months each), intermediate in CBD and DLB (40 and 42 months), and long in PD (84 months). Median dysphagia latencies were intermediate in PSP (42 months), DLB (43 months), CBD (64 months), and MSA (67 months), and long in PD (130 months). Dysarthria or dysphagia within 1 year of disease onset was a distinguishing feature for atypical parkinsonian disorders (APDs) (specificity, 100%) but failed to further distinguish among the APDs. Survival time after onset of a complaint of dysphagia was similar in PD, MSA, and PSP (15 to 24 months, P =.7) and latency to a complaint of dysphagia was highly correlated with total survival time (rho = 0.88; P<.001) in all disorders. CONCLUSIONS: Latency to onset of dysarthria and dysphagia clearly differentiated PD from the APDs, but did not help distinguish different APDs. Survival after onset of dysphagia was similarly poor among all parkinsonian disorders. Evaluation and adequate treatment of patients with PD who complain of dysphagia might prevent or delay complications such as aspiration pneumonia, which in turn may improve quality of life and increase survival time.

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Unique Identifier: 97151878 / PubMed Identifier: 8997827

Authors: Leopold NA. Kagel MC.

Institution: Department of Medicine, Crozer-Chester Medical Center, Upland, Pennsylvania 19013, USA.

Abstract: The radiologic characteristics of pharyngoesophageal (PE) dysfunction in Parkinson's disease (PD) are not well established, partly because most previous studies have examined only small numbers of patients. We administered a dynamic videofluoroscopic swallowing function study to 71 patients with idiopathic PD. Using the Hoehn and Yahr disease severity scale, patients were subdivided into those with mild/moderate disease, subgroup I (n = 38), and advanced PD disease, subgroup II (n = 33). From pharyngeal ingestion to gastric emptying, bolus transport was normal in only 2 patients. The most common abnormalities occurring during pharyngeal ingestion included impaired motility, vallecular and pyriform sinus stasis, supraglottic and glottic aspiration, and deficient epiglottic positioning and range of motion. Esophageal abnormalities were multiple but most commonly included delayed transport, stasis, bolus redirection, and tertiary contractions. Typical aberrations of lower esophageal sphincter (LES) function included an open or delayed opening of the LES and gastro-esophageal reflux. A pathogenesis linking PE with the pathology of PD is proposed.

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Unique Identifier: 96156039 / PubMed Identifier: 8566584

Authors: Ali GN. Wallace KL. Schwartz R. DeCarle DJ. Zagami AS. Cook IJ.

Institution: Department of Gastroenterology, St. George Hospital, University of New South Wales, Sydney, Australia.

Abstract: BACKGROUND & AIMS: Oral-pharyngeal dysphagia in Parkinson's disease is well recognized. The aim of this study was to establish the mechanisms of oral-pharyngeal dysphagia in these patients. METHODS: Using simultaneous videoradiography and pharyngeal manometry, we studied 19 patients with Parkinson's disease (12 with oral-pharyngeal dysphagia and 7 without oral-pharyngeal dysphagia) and compared them with 23 healthy controls. RESULTS: the clinical severity of Parkinson's disease predicted neither the presence nor the severity of dysphagia. Minor alterations in oral function were common in controls and patients, but pharyngeal dysfunction was significantly more prevalent in patients. Incomplete upper esophageal sphincter (UES) relaxation was present in 4 patients (21%), all of whom showed increased hypopharyngeal intrabolus pressure, but not all of whom had a diminished UES opening. The patients had a reduced UES diameter (P = 0.004) and a higher intrabolus pressure compared with the controls (P = 0.007). Pharyngeal contraction pressures were lower in patients, but 6 patients with dysphagia and an abnormal pharyngeal wall motion had normal peak pressures. CONCLUSIONS: An incomplete UES relaxation and a reduced UES opening, both associated with high intrabolus pressure, are prevalent in Parkinson's disease. Oral-pharyngeal dysphagia in Parkinson's disease is multifactorial, with the majority of patients showing oral and pharyngeal dysfunction, even before the clinical expression of dysphagia. Impaired pharyngeal bolus transport is the major determinant of dysphagia.